Cell jamming: Collective invasion of mesenchymal tumor cells imposed by tissue confinement

Haeger, Anna; Krause, Marina; Wolf, Katarina; Friedl, Peter

doi:10.1016/j.bbagen.2014.03.020

Cited by 271 publications

(300 citation statements)

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“…Last, individually moving cells may still engage with other cells in short-lived junctions, which may or may not induce repulsion and directional change, and thereby retain cooperative input from neighboring cells (Ellison et al 2016). As a special case, an otherwise loosely connected cell may upscale cooperativity as part of, for example, a cell-jamming transition when cells are confined in tissue space, and thereby adopt emergent behaviors, including persistent intercellular adhesion and signal integration (Haeger et al 2014;Sarkar et al 2016). Thus, different junction states and environmental conditions enable unique sets of emergent mechanical and signal integration beyond single cell behavior.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, both E-and N-cadherin can orchestrate AJs and cell-cell interactions in cancer cells (Bronsert et al 2014;Zucchini et al 2014). Besides cadherins, Ig superfamily members and ephrins/EpH receptor systems were implicated in mediating more labile or transient cell-cell interactions in cancer cells (Cavallaro and Christofori 2004;Haeger et al 2014;Krusche et al 2016). As well, connexins may enable communication through GJs between connected tumor cells and their inhibition reduces collective migration in prostate cancer cells (Zhang et al 2015).…”

Section: Collective Cell Migration By Cell -Cell Junction Regulationmentioning

confidence: 99%

“…1E) (Scarpa et al 2015). Examples are the migration of neural crest cells in developing embryos, neuronal/astrocyte networks (Scarpa et al 2015), glioma cells retaining filamentous cell -cell interactions while moving through complex brain parenchyma (Osswald et al 2015), and mesenchymal tumor cells moving through confining tissue (Ilina et al 2011;Haeger et al 2014). Collectively, moving loose networks are mediated by complex morphological junctions mediated by N-cadherin for cell-cell adhesion and additional receptors mediating repulsive signals, including Ephrin/Eph receptors (Theveneau and Mayor 2011).…”

Section: Cell-cell Adhesion States and Dynamicsmentioning

confidence: 99%

“…As a consequence, cells coordinate their polarity and respond to extracellular signals as a group, but also retain the remarkable ability of moving individually. Mesenchymal tumor cells develop ALCAM-positive cell-cell junctions when moving through confined space, and gain many properties of collective invasion, including shared migration path, lateral cell-cell junctions, and alignment of front -rear polarity and mitotic planes (Haeger et al 2014). But they also retain the ability to rapidly detach in response to extracellular signals such as growth factors, altered tissue geometry, or matrix metalloproteinase (MMP) availability (Wolf et al 2007;Ilina et al 2011).…”

Section: Cell-cell Adhesion States and Dynamicsmentioning

confidence: 99%

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Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Friedl

Mayor

2017

Cold Spring Harb Perspect Biol

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Collective cell migration critically depends on cell -cell interactions coupled to a dynamic actin cytoskeleton. Important cell-cell adhesion receptor systems implicated in controlling collective movements include cadherins, immunoglobulin superfamily members (L1CAM, NCAM, ALCAM), Ephrin/Eph receptors, Slit/Robo, connexins and integrins, and an adaptive array of intracellular adapter and signaling proteins. Depending on molecular composition and signaling context, cell -cell junctions adapt their shape and stability, and this gradual junction plasticity enables different types of collective cell movements such as epithelial sheet and cluster migration, branching morphogenesis and sprouting, collective network migration, as well as coordinated individual-cell migration and streaming. Thereby, plasticity of cell -cell junction composition and turnover defines the type of collective movements in epithelial, mesenchymal, neuronal, and immune cells, and defines migration coordination, anchorage, and cell dissociation. We here review cell -cell adhesion systems and their functions in different types of collective cell migration as key regulators of collective plasticity.

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Section: Discussionmentioning

confidence: 99%

Section: Collective Cell Migration By Cell -Cell Junction Regulationmentioning

confidence: 99%

Section: Cell-cell Adhesion States and Dynamicsmentioning

confidence: 99%

Section: Cell-cell Adhesion States and Dynamicsmentioning

confidence: 99%

See 2 more Smart Citations

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Friedl

Mayor

2017

Cold Spring Harb Perspect Biol

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307

253

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“…collective cell migration | avalanches | universality | vascular endothelial cadherin | collagen substrate C ollective cell movement depends on intracellular biological mechanisms as well as environmental cues due to the extracellular matrix (1)(2)(3)(4)(5), mainly composed of collagen which is organized in hierarchical structures, such as fibrils and fibers. The mechanical properties of collagen fibril networks are essential to offer little resistance and high sensitivity to small deformations, allowing easy local remodeling and strong strain stiffening needed to ensure cell and tissue integrity (6).…”

mentioning

confidence: 99%

Bursts of activity in collective cell migration

Chepizhko

Giampietro

Mastrapasqua

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Dense monolayers of living cells display intriguing relaxation dynamics, reminiscent of soft and glassy materials close to the jamming transition, and migrate collectively when space is available, as in wound healing or in cancer invasion. Here we show that collective cell migration occurs in bursts that are similar to those recorded in the propagation of cracks, fluid fronts in porous media, and ferromagnetic domain walls. In analogy with these systems, the distribution of activity bursts displays scaling laws that are universal in different cell types and for cells moving on different substrates. The main features of the invasion dynamics are quantitatively captured by a model of interacting active particles moving in a disordered landscape. Our results illustrate that collective motion of living cells is analogous to the corresponding dynamics in driven, but inanimate, systems.collective cell migration | avalanches | universality | vascular endothelial cadherin | collagen substrate C ollective cell movement depends on intracellular biological mechanisms as well as environmental cues due to the extracellular matrix (1-5), mainly composed of collagen which is organized in hierarchical structures, such as fibrils and fibers. The mechanical properties of collagen fibril networks are essential to offer little resistance and high sensitivity to small deformations, allowing easy local remodeling and strong strain stiffening needed to ensure cell and tissue integrity (6). Wound healing is a typical biological assay to study collective migration of cells under controlled conditions in vitro and is a prototypical experimental method to study active matter (7-10). Experiments performed on soluble collagen (11) or other gels (12), micropatterned (13, 14) and deformable substrates (1) show that cell migration is guided by the substrate structure and stiffness (5,15,16).It has been argued that collective migration properties arise from stresses transmitted between neighboring cells (1) giving rise to longranged stress waves in the monolayer (17,18). Hence the dynamics of an invading cell sheet is ruled by a combination of long-range internal stresses and interactions with the substrate, suggesting an analogy with driven elastic systems moving in a disordered medium such as cracks lines (19,20), imbibition fronts (21), or ferromagnetic domain walls (22). The scaling laws in these systems are usually associated with a depinning critical point that has been widely studied by simple models for interface dynamics. Thanks to a combination of numerical simulations (23, 24) and renormalization group theory (23,(25)(26)(27), we now have a detailed picture of the nonequilibrium phase transitions and universality classes in these systems. Here we substantiate the analogy between collective cell migration and depinning by revealing and characterizing widely distributed bursts of activity in the collective migration of different types of cells (human cancer cells and epithelial cells, mouse endothelial cells) over different substrates ...

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Modes of invasion during tumour dissemination

2016

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Cancer cell migration and invasion underlie metastatic dissemination, one of the major problems in cancer. Tumour cells exhibit a striking variety of invasion strategies. Importantly, cancer cells can switch between invasion modes in order to cope with challenging environments. This ability to switch migratory modes or plasticity highlights the challenges behind antimetastasis therapy design. In this Review, we present current knowledge on different tumour invasion strategies, the determinants controlling plasticity and arising therapeutic opportunities. We propose that targeting master regulators controlling plasticity is needed to hinder tumour dissemination and metastasis.

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Cell jamming: Collective invasion of mesenchymal tumor cells imposed by tissue confinement

Cited by 271 publications

References 73 publications

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Tuning Collective Cell Migration by Cell–Cell Junction Regulation

Bursts of activity in collective cell migration

Modes of invasion during tumour dissemination

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